Research shows it is clear that no one single nutrient (with the exception of lithium) can provide a reliably effective treatment for mood disorders. Rather, the evidence implies that a broad range of nutrients are involved in achieving optimum mental stability:
Various micronutrient-related factors are associated with increased risk of psychiatric illness, and micronutrients play essential roles in an array of brain functions that have been implicated in mood lability. Micronutrient inadequacy may impair one or more of these critical brain functions and result in psychiatric symptoms. The micronutrient-mood regulation mechanisms discussed in this review are not exhaustive, nor are they mutually exclusive; in fact, they may be complementary. For example, neurotransmitter production and regulation, key components of the monoamine or chemical imbalance hypothesis of mood disorders, may work in tandem with neurite outgrowth and gene expression of neurotrophic factors, elements of the network hypothesis; these hypotheses appear to be entirely complementary.28
Intestinal disruption and lack of absorption
Gastrointestinal tract disruption appear to deprive the brain of essential nutrients for key metabolic pathways. Gastrointestinal tract disruptions and psychiatric disorders show remarkably high co-morbidity.29 For example, most studies that have investigated the co-morbidity of irritable bowel syndrome and psychiatric disorders show prevalence of psychiatric disorders in irritable bowel syndrome patients to be 90% or greater.30
Higher, genetically-based micronutrient requirements
Research is uncovering major genetic risk factors in psychiatric illness.31 Up to one-third of gene mutations result in decreased enzyme binding affinity for corresponding coenzymes, including vitamins and minerals.32 As a result, individuals with certain genotypes may have significantly higher requirements for essential micronutrients in key mood-related brain pathways.32 33 44
Low micronutrient intake exacerbates the problem
Low micronutrient intake may contribute to psychiatric illness.34 35 36 Intake of many micronutrients is inadequate in the United States, as shown in Figure 2. RDA levels are deemed to be "sufficient to meet the dietary requirements of nearly all (97 to 98 percent) of healthy individuals", but do not ensure mental health for at-risk sub-populations:13 "intake at the level of the RDA or AI would not necessarily be expected to replete individuals previously undernourished, nor would it be adequate for disease states marked by increased requirements."37
Synthesis of neurotransmitters
Many neurotransmitters require micronutrient cofactors in their synthesis. Iron and copper have roles in serotonin and dopamine synthesis.39 40 Folic acid and vitamin B12 are involved as cofactors in serotonin and norepinephrine synthesis.41 Thiamine serves as a coenzyme in acetylcholine, GABA, and glutamate synthesis.42 Vitamin B6 serves as a cofactor in the synthesis of the neurotransmitters dopamine, serotonin, norepinephrine, epinephrine, histamine, and GABA,43 and vitamin B6 deficiency has been shown to reduce brain production of serotonin and GABA.44
Regulation of neurotransmission
Micronutrients play key roles in regulating neuronal transmission. Zinc is extensively involved in synaptic transmission,45 46 both excitatory and inhibitory.47 In certain brain regions, vesicular zinc is co-localized and co-released with glutamate, modulating the function of a number of channels, receptors, and transporters,48 49 including NMDA receptors.50 Magnesium and copper are important modulators of NMDA-receptor activity, which has been implicated in the pathogenesis of mood disorders.51 52
Hypomethylation has been reported as a major risk factor for schizophrenia and bipolar disorder.53 Hundreds of methylation reactions occur in the body, including during DNA, RNA, and neurotransmitter synthesis. The neuropsychiatric effects of folate and vitamin B12 deficiencies result from defective methylation processes.54 55 Folate is a precursor to S-adenosyl-L-methionine (SAMe), a methyl donor that has been shown to have antidepressant properties.56 Choline is also major source of methyl groups for methylation reactions,57 and has been reported to enhance symptoms of patients being treated with lithium.58
Prevention of genetic damage
Deficiency of folic acid, niacin, vitamin B6, vitamin B12, vitamin C, vitamin E, iron, or zinc (one or more of which is seen in half the US population59) have been shown to mimic radiation in causing single- and double-strand DNA breaks, which could decrease enzyme affinity for nutrient cofactors.60 61 Folate deficiency of a magnitude seen in 10% of the US population breaks chromosomes by causing massive mis-incorporation of uracil into human DNA.59 In addition, various vitamin and mineral deficiencies have been shown to accelerate mitochondrial decay, leading to DNA damage.62
Various micronutrients are involved in gene expression. Folate plays an essential role in methylation, which is involved in gene expression, transcription, chromatin structure, genomic repair and genomic stability.63 Vitamin A and vitamin E have been reported to have roles in gene expression as well.64 65 Vitamin D, zinc and calcium have been shown to be involved in brain-derived neurotrophic factor (BDNF) gene expression, an effect also seen in clinically effective antidepressants.66 67 68 69 TrkB, a BDNF-activated receptor, has been shown to be activated by zinc and copper.70 71
Several micronutrients have been shown to be involved in neurite outgrowth, which is critical in optimizing neural networks. Vitamin A is a precursor to retinoic acid, which is extensively involved in neurite outgrowth and axonal elongation.72 73 Calcium plays critical roles in neurite outgrowth.74 75 76 Magnesium, selenium, and copper are also involved.77 78 79
Recent clinical trials using non-lithium micronutrient interventions have shown beneficial effects on mood. Multi-micronutrient interventions appear to be particularly promising. Certain sub-populations may have increased requirements for micronutrients, which are extensively involved in an array of mood-related brain functions. Micronutrient inadequacy may impair one or more critical brain functions, resulting in psychiatric symptoms.
Micronutrient inadequacy impairs mood-related brain function, resulting in psychiatric symptoms. When patients in research samples have multiple micronutrient inadequacies (USDA data38), single-nutrient interventions may show only marginal effects; multiple-nutrient interventions, however, result in more complete, dramatic effects. The concept of multiple-micronutrient inadequacy may explain why clinical trials using single-nutrient interventions show only marginal effects. A broad-spectrum multi-ingredient treatment is required to test the hypothesis that micronutrient inadequacy impairs key brain functions and produces psychiatric symptoms.
Environmental and Genetic Pressures on Brain Functions (PDF)
To understand what makes EMPowerplus™ so effective for bipolar, depression, and other mood disorders, it’s important to recognize the relationship between micronutrient deficiencies and the incidence of mental illness. For example, research on the role of zinc in depression showed that levels of zinc in the blood of depressed subjects was significantly lower than in controls.
Could micronutrient deficiencies be affecting your mental health?
Despite efforts to eat a balanced diet with healthier food choices, this graph from the USDA shows most Americans do not meet the Recommended Daily Allowance (RDA) for many essential micronutrients. This may be one reason why the incidence of mental illness and mood disorders such as bipolar continue to rise at an alarming rate.
The good news? Current research suggests many symptoms of bipolar, depression, anxiety, and ADHD can be reduced or eliminated using the full-spectrum micronutrient formulation of EMPowerplus.
The role of serotonin in mood stability
The “feel good” neurotransmitter serotonin plays a critical role in mood regulation. Most pharmaceutical treatments for depression are known as Selective Serotonin Re-uptake Inhibitors, or SSRIs, and are supposed to keep the mood-balancing effects of serotonin working in the brain longer by blocking its re-absorption in the body.
A better way to look at the role of serotonin is to understand how the body creates this essential neurotransmitter. The following diagram details the chemical reactions the body must go through to produce serotonin and demonstrates that:
The result? Your mood improves and you feel better.
Micronutrient deficiencies can prevent production of other natural chemicals
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